Hypertensive coronary microvascular dysfunction: a subclinical marker of end organ damage and heart failure

Abstract

<jats:title>Abstract</jats:title> <jats:sec> <jats:title>Aims</jats:title> <jats:p>Hypertension is a well-established heart failure (HF) risk factor, especially in the context of adverse left ventricular (LV) remodelling. We aimed to use myocardial flow reserve (MFR) and global longitudinal strain (GLS), markers of subclinical microvascular and myocardial dysfunction, to refine hypertensive HF risk assessment.</jats:p> </jats:sec> <jats:sec> <jats:title>Methods and results</jats:title> <jats:p>Consecutive patients undergoing symptom-prompted stress cardiac positron emission tomography (PET)-computed tomography and transthoracic echocardiogram within 90 days without reduced left ventricular ejection fraction (&amp;lt;40%) or flow-limiting coronary artery disease (summed stress score ≥ 3) were included. Global MFR was quantified by PET, and echocardiograms were retrospectively analysed for cardiac structure and function. Patients were followed over a median 8.75 (Q1–3 4.56–10.04) years for HF hospitalization and a composite of death, HF hospitalization, MI, or stroke. Of 194 patients, 155 had adaptive LV remodelling while 39 had maladaptive remodelling, which was associated with lower MFR and impaired GLS. Across the remodelling spectrum, diastolic parameters, GLS, and N-terminal pro-B-type natriuretic peptide were independently associated with MFR. Maladaptive LV remodelling was associated with increased adjusted incidence of HF hospitalization and death. Importantly, the combination of abnormal MFR and GLS was associated with a higher rate of HF hospitalization compared to normal MFR and GLS [adjusted hazard ratio (HR) 3.21, 95% confidence interval (CI) 1.09–9.45, P = 0.034), including in the adaptive remodelling subset (adjusted HR 3.93, 95% CI 1.14–13.56, P = 0.030).</jats:p> </jats:sec> <jats:sec> <jats:title>Conclusion</jats:title> <jats:p>We have demonstrated important associations between coronary microvascular dysfunction and myocardial mechanics that refine disease characterization and HF risk assessment of patients with hypertension based on subclinical target organ injury.</jats:p> <jats:p /> </jats:sec>

Coronary Microvascular Dysfunction

“…While a small proportion of patients with LV hypertrophy undergo myocardial infarction developing LV dilatation and heart failure, most patients progress directly to heart failure [ 187 ]. Abnormalities in microvascular function, structure, and perfusion may be responsible for the transition from hypertensive heart disease to LV dysfunction and heart failure in patients without epicardial CAD [ 188 , 189 ]. Microvascular rarefaction, perivascular fibrosis, and medial thickening of arterioles with reduced luminal areas have been observed in patients with hypertension without obstructive CAD [ 190 , 191 ].…”

The year in cardiovascular medicine 2020: heart failure and cardiomyopathies

“…26 Myocardial mechanics is linked to coronary microvascular dysfunction in patients with hypertensive HF. 27,28 In AHF, cardiac sympathetic nerve dysfunction, as evaluated by 123 I-metaiodobenzylguanidine imaging, is associated with poor outcome irrespective of LVEF. 29…”

Association of urine albumin‐to‐creatinine ratio with subclinical systolic dysfunction in hypertensive patients but not normotensive subjects: Danyang study

“…27 More importantly, a recent study demonstrated significant associations between CMD and impaired GLS and future HF risk in hypertensive patients. 28 Although higher UACR was significantly associated with worse diastolic dysfunction defined by lower e′ and higher E/e′, these relationships were attenuated after multivariable adjustment. There are conflicting findings with respect to the association between UACR and diastolic function.…”

“…Indeed, CMD was associated with a markedly increased risk of HFpEF 27 . More importantly, a recent study demonstrated significant associations between CMD and impaired GLS and future HF risk in hypertensive patients 28 …”